ArticleOncoimmunology2025
Co-targeting of VEGFR2 and PD-L1 promotes survival and vasculature normalization in pleural mesothelioma.
Article in Oncoimmunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Comparative Gene Expression Analysis of Epithelioid Pleural and Peritoneal Mesothelioma.Cancers · 2026Article
- Immune Roles of Canonically Non-Immune Cells in Biomaterials Response.Cell biomaterials · 2026Article
- The tumor microenvironment: a dynamic ecosystem and therapeutic nexus in modern oncology.Frontiers in pharmacology · 2026Review
- Immunotherapy resistance and strategies in malignant pleural mesothelioma.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Review
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pleural mesothelioma (PM) is an aggressive cancer caused by asbestos exposure, with limited treatment options and poor prognosis, highlighting the need for more effective therapies. Combining immune checkpoint blockade with anti-angiogenic therapy has shown potential in other cancers. Our study investigated the combined inhibition of PD-L1 and VEGFR2 in a mouse model of PM. Using C57BL/6 mice with subcutaneous AE17 mesothelioma tumors, we assessed the effects of anti-PD-L1 therapy with induction, concomitant, or consolidation anti-VEGFR2 treatment. Mice received intraperitoneal doses every three days for three treatments. Tumor growth, survival, tumor-infiltrating immune cells and intra-tumoral vasculature were analyzed. Results demonstrated that combining anti-PD-L1 with induction or concomitant anti-VEGFR2 significantly delayed tumor growth, improved survival, and promoted vascular maturation. Flow cytometry suggested T cell exhaustion in monotherapy groups, while no significant changes were seen with concomitant treatment. Depleting CD4
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